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Title: [Vaspin protects against lipopolysaccharide-induced acute respiratory distress syndrome in mice by inhibiting inflammation and protecting vascular endothelium via PI3K/Akt signal pathway].
Author: Li W, Qi D, Chen L, Zhao Y, Deng W, Tang XM, Wang DX.
Journal: Nan Fang Yi Ke Da Xue Xue Bao; 2018 Mar 20; 38(3):283-288. PubMed ID: 29643033.
Abstract:
OBJECTIVE: To investigate the effects of Vaspin on lipopolysaccharide (LPS)-induced acute respiratory distress syndrome (ARDS) in mice and explore the possible mechanism. METHODS: Forty male C57B/L6 mice were randomized equally into control group, LPS group, Vaspin group and wortmannin group with corresponding treatments. The pathological changes of the lung tissues were evaluated by HE staining, and the severity of pulmonary edema was measured according to the wet/dry ratio (W/D) of the lung tissue. The lung permeability was evaluated by detecting total protein concentrations in the bronchoalveolar lavage fluid (BALF) using bicinchoninic acid (BCA) assay. Myeloperoxidase (MPO) activity in the lung tissue was detected using a MPO assay kit, and the levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the lungs were measured using ELISA. Immunohistochemical staining was performed to detect the expression of vascular cell adhesion molecule-1 (VCAM-1) and Western blotting was used to detect the protein expressions of cleaved caspase-3 and p-Akt in the lung tissues. RESULTS: Compared with the control group, the mice in LPS group displayed typical ARDS pathological changes in the lungs with significantly increased W/D, total protein concentrations in BALF, lung MPO activity, levels of IL-1β and TNF-α, and pulmonary expressions of VCAM-1 and cleaved caspase-3 (P<0.05) but decreased expression of p-Akt (P<0.05). These changes induced by LPS were significantly alleviated by the administration of Vaspin (P<0.05). The protective effects of Vaspin against ARDS were obviously attenuated by the PI3K inhibitor wortmannin (P<0.05). CONCLUSION: Vaspin protects against LPS-induced ARDS in mice possibly by inhibiting inflammation and protecting vascular endothelium through upregulation of the PI3K/Akt signal pathway. 目的: 探讨Vaspin对LPS致ARDS小鼠的保护作用及其可能机制。方法: 40只雄性C57BL/6J小鼠按随机数字表分为对照组、LPS组、Vaspin组和wortmannin（PI3K抑制剂）组，每组10只。苏木精-伊红（HE）染色观察肺组织病理改变，肺湿干比评估肺水肿，BCA法检测支气管肺泡灌洗液（BALF）中蛋白含量，评估肺组织通透性改变；髓过氧化物酶（MPO）试剂盒检测肺组织MPO活性，ELISA检测肺组织中白细胞介素（IL-1β）和肿瘤坏死因子（TNF-α）的含量，免疫组织化学法（IHC）观察肺组织中VCAM-1表达；Western blot法检测肺组织cleaved caspase-3和Akt磷酸化水平。结果: 与对照组比较，LPS组小鼠肺组织呈现典型ARDS病理改变，肺组织湿干比W/D值、BALF蛋白含量、肺组织MPO活性、IL-1β和TNF-α水平，肺组织VCAM-1表达及cleaved caspase-3蛋白表达水平显著增高（P < 0.05），而p-Akt蛋白表达明显下调（P < 0.05）；Vaspin干预能显著缓解上述变化（P < 0.05）；而wortmannin组与Vaspin组相比，其湿干比W/D值、BALF蛋白含量、MPO活性和IL-1β、TNF-α及cleaved caspase-3蛋白表达水平显著升高（P < 0.05），伴Akt磷酸化水平显著下调（P < 0.05）。结论: Vaspin可通过其介导的抗炎、抗凋亡及血管内皮保护效应对LPS致ARDS肺损伤发挥保护性调控，其可能机制为上调了PI3K/Akt通路。

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